Salmonella continues to be a major public health burden worldwide. Poultry are known to be one of the main reservoirs for this zoonotic pathogen. It has previously been shown that a single dose of Bacillus subtilis reduces fecal shedding of Salmonella enterica serovar Enteritidis, whereas no effect on long-term colonization of the cecum has been observed. Here we report experiments that were undertaken to test the efficacy of a conventional diet supplemented with a probiotic (B. subtilis DSM17299) on 1) Salmonella colonization in the intestinal tract of broiler chickens, and 2) fecal shedding of Salmonella under production-like conditions. The trial birds fed the B. subtilis diet showed a significant 58% reduction in Salmonella-positive drag swabs compared with control birds, which had 100% presence of Salmonella. Feeding B. subtilis significantly reduced the average Salmonella load of cecum samples of the chickens, by 3 log units. This reduction in Salmonella colonization might not only positively affect broilers on the live production side by reducing the risk of infection between birds, but could also aid on the processing side by decreasing the amount of Salmonella entering the facility and improving food safety. Furthermore, numerical, but not statistically significant, improvements in feed conversion rate and BW gain at d 42 were observed in the B. subtilis-treated group compared with control birds.

Our investigations concerning the importance of cell surface macromolecules during embryonic development led us to the discovery in 1961 that heterologous anti-rat kidney serum produced teratogenesis, growth retardation and embryonic death when injected into the pregnant rat during early organogenesis. It was established that IgG was the teratogenic agent, primarily directed against the visceral yolk sac (VYS) but not the embryo. Heterologous anti-rat VYS serum was prepared which was teratogenic localized in the VYS and served as a model for producing VYS dysfunction and embryonic malnutrition. The role of the yolk sac placenta in histiotrophic nutrition is now recognized to be critical for normal embryonic development during early organogenesis in the rodent. VYS antiserum affects embryonic development primarily by inhibiting endocytosis of proteins by the VYS endoderm, resulting in a reduction in the amino acids supplied to the embryo. Our laboratory has recently developed teratogenic monoclonal yolk sac antibodies (MCA) which can be utilized; to study VYS plasma membrane synthesis and recycling, to compare yolk sac function among different species, and to identify components of the plasma membrane involved in pinocytosis. MCA prepared against certain VYS antigens provide an opportunity to study embryonic nutrition with minimal interference with the nutritional state of the mother. Recent developments in the study of the human yolk sac along with our laboratory's ability to isolate a spectrum of yolk sac antigens, prepare monoclonal antibodies, and perform functional studies, should provide information that will increase our understanding of yolk sac function and dysfunction in the human and determine the relative importance of various amino acids to normal development during mammalian organogenesis.

The visceral yolk sac (VYS) is an especially important placental organ in the rodent because it is the primary source of exchange between the embryo and mother during early organogenesis before the chorioallantoic placenta circulation is established. The VYS is involved with nutritional, endocrine, metabolic, immunologic, secretory, excretory, and hematopoietic functions. The VYS also plays a role in steroid metabolism and interacts with a variety of blood-borne factors: parathyroid hormone, glucocorticoids, insulin, and vitamin D metabolites. The importance of the VYS during development is emphasized by the embryotoxicity resulting from exposure to agents which cause VYS dysfunction when administered to the pregnant animal during organogenesis. Several experimental procedures have provided useful information concerning a variety of VYS functions from early organogenesis to term: Culture of the Embryo, Fetal Incubation, Culture of the Fetus, Giant Yolk Sac, Short- and Long-Term Culture of the Yolk Sac, Modified Ussing's Chamber, Single or Double Diffusion Chamber, and the use of Heterologous Rodent Visceral Yolk Sac Antibodies. Since human yolk sac pathology has been associated with developmental toxicity and spontaneous abortion, it is important to discover whether there are some common functional roles among different mammalian species and to determine if other experimental animal models can be used to study the possible contribution of human yolk sac dysfunction to some human reproductive problems.

Staphylococcus aureus and various coagulase-negative staphylococci were isolated from turkeys with staphylococcosis. Virulent S. aureus adhered well (averaged more than 100 bacteria per tissue cell) in vitro to cells from tissues of the respiratory tract but did not adhere well (averaged fewer than 12 bacteria per tissue cell) to cells from tissues of the alimentary tract. Some avirulent coagulase-negative staphylococci also adhered well to cells from the respiratory tissues. Lungs and livers of turkeys became colonized with virulent S. aureus following experimental aerosol exposure. Tracheas, livers, and hock joints of some market-age turkeys were naturally colonized with S. aureus and various species of coagulase-negative staphylococci.

Heterologous antisera against rat yolk sac made in rabbits and sheep produced congenital malformation, fetal growth retardation, and embryonic death when injected into pregnant rats. Antigens present in the cellular or acellular portions of the yolk sac were capable of producing teratogenic antibodies. Fluorescence-labeling techniques revealed that yolk-sac antiserum contained antibodies that reacted strongly with the nonserum-protein antigens of maternal adrenal, ovary, and kidney; fetal yolk sac; and chorioallantoic placenta. Teratogenic yolk-sac antiserum localized in the noncellular and intracellular portions of the parietal and visceral yolk sac including Reichert's membrane. It is postulated that yolk-sac dysfunction is produced by the localization of these antibodies in the yolk sac. The localization of yolk-sac antiserum in the yolk sac was observed at term regardless of whether the antiserum was injected on the 11th or 20th day of gestation, although the time of injection affected the localization at term qualitatively and quantitatively. These results suggest that further studies of the functions of the yolk sac at various periods of gestation are indicated not only in rodents but in humans since the yolk sac may play a role in human teratogenesis. The unanswered questions concerning yolk-sac function and dysfunction in rodents and the importance of the yolk sac in humans add another aspect to the problem of transferring the results of teratogenic studies in rodents to the human situation.